Moreover, c-Jun stimulates melanoma dedifferentiation and inflammatory cytokine production via counteraction with MITF, resulting in the recruitment of immune suppressive myeloid cells into the tumor microenvironment.63 Lastly, JNK/c-Jun inhibition with a peptide inhibitor inhibits melanoma growth in mouse, and attenuates cancer induced pain hypersensitivity.64 Thus, JNK/c-Jun promotes tumor cell growth and progression through both cell intrinsic and extrinsic mechanisms. This evidence concerns the gene JUN and cancer.